PATTERN BASED EVALUATION OF ILD
a.
History and Labs
i. Age
(20-40yo=sarcoid, EG, CVD; consider IPF in >50yo)
ii.
Sex (LAM exclusively in women)
iii.
Smoking hx (smokers=EG, RB/RBILD/DIP;
non-smokers=HP, sarcoidosis)
iv.
Time course (acute onset=AIP)
v. Family
hx (LAM, sarcoidosis)
vi.
Exposure/toxins (pets/hobbies/occupation/home
environment)
vii.
CVD (RA, scleroderma etc)
viii.
Malignancy
ix.
Symptoms (no extrapulm sxs in IPF; CP pleurisy
in CVD)
x. Labs
(PFTS with DLCO, ANA, RF, ANCA, anti-BM ab, cryoglobulins, hypersensitivity
panel)
b.
Location/distribution
i. Focal
vs patchy vs diffuse
ii.
Upper, middle, lower lobe pre-dominant (vs
panlobar)
iii.
Peripheral vs central vs peribronchovascular
(sarcoid, lymphangitic spread, LIP, lymphoma or lymphoproliferative d/o,
amyloid)
iv.
Reticular, reticulonodular, micronodular
v. What
is “fibrosis”? intra-lobular septal thickening (fine reticulation), traction
bronchiectasis, honeycombing all are considered fibrosis
c. Lines
i. Peripheral
reticular pattern if lower lobe
predominant
1.
UIP
2.
Fibrotic NSIP assoc with chronic CVD (esp
scleroderma) and RA (distal clav absorption)
3.
Drug toxicity (BAM=bleomycin, amiodarone,
methotrexate)
4.
Asbestosis (parenchymal bands and curvilinear
subpleural lines)
5.
Chronic emphysema (smoking-related interstitial
dz)
ii.
linear pattern (aka lines radiating
from hila +/- kerley lines) “LIFE”
1.
Lymphagitic spread
2.
(Atypical) infection like viral/mycoplasma
3.
Fibrosis like IPF
4.
Edema
iii.
Septal thickening
1.
Intra-lobular (fine reticular=fibrosis)
2.
Inter-lobular septal thickening (secondary
lobules)—if not the predominant finding, can ignore this!!
a.
Smooth septal thickening (water=edema,
pus=infx, blood=hemorrhage, protein=PAP)
b.
Nodular septal thickening (sarcoid,
lymphangitic spread, LIP, lymphoma or lymphoproliferative d/o, amyloid)
c.
Irregular (any fibrosing lung dz)
iv.
Subpleural lines or parenchymal bands
(scarring/fibrosis, atelectasis, asbestosis)
d. Nodules
i. Micronodules
(<3-5mm)
1.
Centrilobular (evenly spaced, don’t extend to
pleura or fissure)
a.
GG (ill-defined)
i. HP
subacute in non-smoker (classic), hemosiderosis
ii.
RB or RBILD in smokers (“subtle GG nodules” in
smokers)
iii.
Associated with NSIP (CVD) and OP/COP
b.
Solid with TIB (90% infectious
bronchiolitis)
i. Think
inflammatory /infectious bronchiolitis vs Aspiration
1.
STAB= smokers, TB/MAI, Aspiration,
Bronchiolitis, BAC (endobronchial adenoCA), BronchoPNA (patchy clustered
nodules)
ii.
If central mucus plugging (finger-in-glove),
consider asthma, CF, ABPA
iii.
Mimicker=tumor emboli (branching tumor in
enlarged vessel in peribronchovascular distribution)
iv.
AIDS-related airways disease
v. Endobronchial
mucinous adenoCA (BAC)
c.
Solid without TIB
i. Pneumoconiosis/Silicosis
(look for PMF etc)
ii.
EG (aka pulm LCH)--if nodules are dense; may
cavitate
2.
Perilymphatic (patchy and abut pleura
and fissure)
a.
Sarcoid, lymphangitic spread, LIP, lymphoma or
lymphoproliferative d/o, amyloid
3.
Random (aka miliary; diffuse/uniform unlike
perilymphatic)
a.
METS-B=hematogenous mets
(thyroid/renal/melanoma), EG, miliary TB/fungal/disseminated viral,
sarcoid/silicosis, BAC
ii.
Branching nodules within enlarged vessel in
peribronchovascular distribution = consider tumor emboli
e. GGO (can see vessels thru it)
i. Differential
similar to consolidation
ii.
“ABCDEH”= PAP, BOOP/COP, PCP,
DIP, Drugs, Edema, HP, Hemorrhage
iii.
Acute
vs chronic
1.
Acute GGO
a.
Edema (CHF and in ICU pts consider
ARDS/DAD/AIP)
b.
Hemorrhage (hemosiderosis)
c.
Atypical infx (PCP in AIDS and CMV in
post-transplant)
d.
Subacute HP (“head-cheese”)
2.
Chronic GGO
a.
PAP (“crazy paving”=geographic GG with septal
thickening), PCP (UL cysts and perihilar GG in HIV pt)
b.
BOOP/COP (peribronchial and subpleural “polygonal”
fleeting consolidations, GGO, and nodules)
c.
DIP and NSIP
d.
Drugs (BAM=bleomycin, amiodarone,
methotrexate)
e.
HP (exposure)
f.
BAC
iv.
Crazy paving ddx= PAP, pulm edema, pulm
hemorrhage, drug-induced pneumonitis, PNA (bacterial like mycoplasma etc),
BAC, COP
v. History
helps
1.
Hemoptysis=hemorrhage
2.
Immunocompromised=infx (PCP)
3.
Exposure=HP (non-smoker)
4.
CVD or ILD=alveolitis
f. Mosaic attenuation
i. How
to tell from GGO=Geographic (sharply demarcation on inspiratory view),
differential vessel size (smaller in lucent areas), air-trapping (on
expiration dark areas remain dark), stable over time
ii.
Note: Mosaic attenuation is an INSPIRATORY
HRCT finding while air-trapping is a EXPIRATORY HRCT findings!!
iii.
small airways disease vs small vessel
disease à
do expiratory view to distinguish btwn the two
iv.
SMALL VESSEL DISEASE (less common) =no
air-trapping; larger areas of non-lobular lucencies with normal vessel size;
pulm HTN and R heart enlargement
1.
Chronic PE (look for associated pulm HTN)
2.
Vasculitis (CVD)
v. SMALL
AIRWAYS DISEASE =with air-trapping; lobular areas of lucencies with small
vessel size; peribronchial thickening
1.
PFTs=decreased VC; decreased FEV1; increased
RV; normal FEV1/VC ratio; normal TLC
2.
Direct signs of small airways dz=bronchial wall
thickening, bronchiolectasis, centrilobular nodules with TIB
3.
Indirect signs of small airways disease dz=
mosaic attenuation (described in inspiration), air-trapping (described in
expiration; mosaic attenuation persists and contours get even more sharply
marginated)
4.
Bronchiolitis
a.
Smokers (RB, RBILD)
b.
Infectious (viral in kids like
RSV/adenovirus/mycoplasma; MAC/TB/fungal in adults)
i. Swyer
James (recurrent viral infx in kids <8yo; unilateral hyperlucent small
lung identified on CXR)
c.
Diffuse panbronchiolitis (exclusively
Japanese)
d.
Follicular bronchiolitis (CVD like sjogrens,
RA, HIV)
5.
B.O./constrictive bronchiolitis (swyer
james in kids <8yo with unilat hyperlucent small lung identified on CXR)
a.
Etiology:
i. Recurrent
viral infx (including mycoplasma)
ii.
Toxic fume exposure (smoking, NO2 silo worker,
SO2, popcorn worker diacetyl)
iii.
Drugs like penicillamine
iv.
CVD, RA
v. Chronic
transplant rejection (after lung transplant or GVHD after BM transplant)
b.
Features
i. Hyperlucent
lobe/lung on inspiration
ii.
Bronchial dilation and peribronchial
thickening (due to constriction of distal bronchioles)
iii.
Air-trapping only seen upon expiration (mosaic attenuation)
6.
Bronchitis
vi.
MOSAIC ATTENUATION without centrilobular
nodules or TIB
1.
Smokers
2.
Asthma, chronic bronchitis
3.
HP
4.
Follicular bronchiolitis
5.
B.O.
vii.
AIR TRAPPING ON EXPIRATORY VIEW
1.
Expiratory view is useful as it can detect
air-trapping which can help with diagnosis of small airways disease
2.
3 patterns
a.
With normal inspiratory CT
i. Normal
patient (≤3 adjacent secondary lobules)
ii.
Asthma and chronic bronchitis
iii.
B.O. (cryptogenic; post-infx like viral or
mycoplasma; toxic inhalation; GVHD; lung transplant; RA; IBD; pencillamine
therapy)
b.
With abnormal inspiratory CT (interstitial
lung changes)
i. Emphysema
ii.
HP
iii.
Sarcoidosis
iv.
Toxic inhalation
v. LAM,
EG
vi.
Others rare stuff like HIV and Churg strauss
c.
With abnormal inspiratory CT (bronchiectasis)
i. CF
ii.
ABPA
iii.
MAI
iv.
Swyer James
v. Chronic
aspiration
vi.
Tracheobronchomalacia
g. Consolidation or airspace disease
i. Diffuse
airspace dz (*=acute)
1.
*water=CHF/ARDS (STD=shock, sepsis, trauma,
drugs like crack cocaine)
2.
*pus=PNA
3.
*blood=hemorrhage (wegners, goodpasture,
hemosiderosis)
4.
cells=lymphoma/BAC/OP
5.
fat=lipoid PNA
6.
protein=PAP
ii.
Upper-lobe predominant= “CASSET-P”
cystic fibrosis, ank spond, sarcoidosis/silicosis, EG, TB, PCP
iii.
Peripheral consolidation= “AEIOU”
alveolar sarcoid, chronic Eos PNA, infarct, OP/COP, UIP
iv.
Migratory/fleeting infiltrates= ABC
acute eos PNA, ABPA, Aspiration, BOOP/COP, Chugg Straus (kids)
v. Dense
consolidations= amiadarone, talcosis (IV drug abuse), PMF
(sarcoid/silicosis), amyloidosis, asbestos plaques (mimicker on CXR)
vi.
Chronic infiltrates= BALLS
BAC/lymphoma, Alveolar sarcoid, lipoid PNA/PAP, sequestration, chronic eos
PNA
vii.
Interstitial infiltrate=LIFE lymphangitic
spread (adenoCA), infx (viral/atypical PNA), fibrosis (IPF), edema
viii.
Infiltrate in kids= round PNA, plasma
cell granuloma, CCAM, CLE, CDH, sequestration, duplication cyst, mets
h. Cysts/Cavitation
i. Emphysema
(blebs vs bullae)
1.
Centrilobular vs Panlobular (lower lobe
predominance; α-1-antitrypin def)
2.
Paraseptal
3.
Cicatricial (assoc with scarring or PMF)
ii.
Cysts
1.
Blebs (<1cm), bullae (>1cm),
pneumatocele
2.
Cavitation
a.
Wall thickness
i. <4mm
(93% b9)
ii.
4-15mm (50% b9 and 50% malignant)
iii.
>16 mm (99% malig)
b.
Inner wall appearance
i. Smooth
(non-specific)
ii.
Nodular=CA
iii.
Shaggy=infx
c.
DDX cavitary lesions= “CT-SWAP” ca
(primary SCC or secondary SCC like H&N males and cervical females),
TB/fungal, septic emboli (feeding vessel sign), wegners (sinusitis) / RA
(necrobiotic), abscess, aspergillosis (GG halo), papillomatosis, others
(sarcoid, EG or PLCH, infarct), cystic bronchiectasis
d.
DDX cystic lesion with increased lung
volumes= EG (male smokers >30yo), LAM (young females), CF, bullous
emphysema, cystic bronchiectasis
e.
DDX thick cavity cyst with debris= infx
(necrotizing PNA with pulm gangrene; TB/sarcoid/CF with mycetoma), infarct,
CA, hydatid
f.
DDX cystic lesion kid= CLE, CCAM
(I/II), CDH, bronchogenic cyst, pneumatocele, cavitary PNA/abscess/TB
iii.
Bronchiectasis
1.
Cylindrical vs varicose (beaded) vs cystic
(saccular)
2.
Bronchiectasis ddx
a.
Recurrent infx/aspiration (like TB, MAI=lady
widemere)
b.
Finger-in-glove=CF/ABPA
c.
Congenital=immotile cilia (kartageners)/william-campbell (Mounier Kuhn=tracheobronchomegaly)
d.
Fibrosis=traction bronchiectasis
e.
Emphysema
iv.
Honeycombing
1.
Associated with interface sign=irreg margins
of pleural and vessels; associate with traction bronchiectasis (corkscrew)
2.
Honeycombing ddx: “SCHARD”=sarcoidosis, CVD,
chronic HP, asbestosis, RA, drug toxicity
3.
Lower lobe fibrosis= UIP or IPF,
fibrotic NSIP assoc with chronic CVD (esp scleroderma), drug toxicity (“BAM”=bleomycin,
amiodarone, methotrexate), asbestosis (parenchymal bands and curvilinear
subpleural lines), RA (distal clav absorption), chronic emphysema
4.
End-stage lung dz= UIP, CVD (esp
scleroderma), sarcoid, chronic HP, asbestosis, RA
i. Others
i. Air-trapping
(emphysema, BO/swyer james, LAM, EG, CF)
ii.
LN (not uncommon in IPF esp if <15mm and
only involves 1-2 nodal stations like paratracheal or subcarinal; usually
responds to therapy like steroids)
1.
Low density LAD= TB/MAI,
wipples/crohns, untreated lymphoma, mets (testicular etc)
2.
High density LAD= castlemans,
carcinoid, Kaposi, LN mets from RCC (hemorrhage)
3.
Calcified LAD= TB, sarcoid/silicosis, treated
lymphoma, papillary thyroid CA
iii.
Effusion (pleural/pericardial)—think CVD or RA
iv.
HIV “please test my CDfour”
1.
CD4>200: candida/Kaposi/TB (secomdary)
2.
CD4<200: PCP, TB (primary)
3.
CD4<100: Toxo
4.
CD4<75: MAC
5.
CD4<50: CMV/PMLE/Fungal
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